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Biomedical subjects

D Rennie

Publications and source records attributed to D Rennie.

At least 91 records · Page 5Linked to original sources
PubMed1991

Effects of slow ascent to 4559 M on fluid homeostasis.

Since acute mountain sickness (AMS) is associated with rapid ascent and with fluid retention, we assessed clinical status and fluid homeostasis in men slowly ascending on foot over 3 d to 4559 m and remaining at this altitude 5 d. We studied 15 male mountaineers, 6 of whom had previously had repeated, severe AMS or high altitude pulmonary edema (HAPE), at 1170 m, 3611 m, and 4559 m. We found that four of the six subjects with previous AMS or HAPE compared with none of nine with no such history, developed these conditions. Those who remained well had a diuresis that could not be overcome by increasing fluid intake and no change in renin activity, plasma aldosterone, or atrial natriuretic peptide (ANP). Those who became ill showed considerable weight gain independent of fluid intake, and a great increase in ANP which correlated with measurements of right atrial cross section. We conclude that mountaineers who have previously experienced repeated AMS or HAPE get fluid retention despite slow ascent and that this is associated with widening of the atrium and an increase in ANP.

Adult↗
PubMed1988

Dexamethasone for prevention and treatment of acute mountain sickness.

We wished to determine in a field study the effectiveness of dexamethasone for prevention and treatment of acute mountain sickness (AMS). Prevention Trial: We transported 15 subjects from sea level to 4,400 m (PB = 400 mm Hg) on Denali (Mt. McKinley) by means of a 1-h helicopter flight. In a randomized, double-blind fashion we gave eight subjects a placebo and seven subjects 2 mg dexamethasone orally every 6 h, starting 1 h before take-off. The entire placebo group and five of the dexamethasone group developed AMS within 5 h, and became progressively more ill until 12 h when the trial was terminated. We concluded that 2 mg of dexamethasone every 6 h did not prevent AMS in active soldiers rapidly transported to high altitude. Treatment Trial: We treated 11 of those with moderate to severe AMS (symptom score 4.5 +/- 0.7, range 3 to 11) with 4 mg of dexamethasone every 6 h orally or intramuscularly for 24 h. All were markedly improved at 12 h (symptom score 1.0 +/- 0.3, p less than 0.001, range 0 to 3), but symptoms increased after the drug was discontinued at 24 h (symptom score = 2.4 +/- 0.5). We conclude that dexamethasone in a dosage of 4 mg PO or IM every 6 h is an effective treatment for AMS, but that illness may recur with abrupt discontinuation of the drug.

Adult↗
PubMed1985

"Bubble Boy'.

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Ethical Review↗
PubMed1983

The composition of a mucus glycoprotein from meconium of cystic fibrosis, healthy pre-term and full-term neonates.

A high molecular mass mucus glycoprotein fraction (molecular mass greater than 1 million) which is a major component of meconium mucin, has been isolated from individual specimens collected from 20 healthy full-term infants, 19 premature infants and 19 infants with proven cystic fibrosis. The mucus glycoprotein fraction isolated from cystic fibrosis meconium had a significantly lower saccharide content than that isolated from specimens from healthy full-term infants but had a similar composition to that isolated from meconium of premature infants, gestational age 28-32 weeks. The composition of the glycoprotein fraction from the meconium of infants, gestational age 32-36 weeks, lay between that from cystic fibrosis and full-term. There is therefore a change or 'maturation' of epithelial mucin during gestation and it is hypothesised that the cystic fibrosis genetic lesion affects the maturation of epithelial secretion, resulting in the abnormal exocrine secretion associated with the disease.

Carbohydrates↗
PubMed1982

Fluid retention and relative hypoventilation in acute mountain sickness.

The presence of pulmonary, cerebral, and/or peripheral edema in acute mountain sickness (AMS) implies a derangement in the body's handling of water. Previously, we demonstrated water retention and increased symptoms of AMS when hypocapnia was prevented in subjects exposed to simulated high altitude. This led us to the hypothesis that upon ascent to high altitude, those persons who fail to increase their ventilation adequately and hence do not become hypocapnic will retain water reflected as weight gain and will develop AMS. To test this hypothesis, we studied in Kathmandu, Nepal (1,377 m) 42 healthy western tourists; all were restudied in Pheriche (4,243 m) within 6 days of exposure to high altitude. Symptoms of AMS were highly correlated (p less than 0.001) with weight change, suggesting that persons becoming symptomatic retained fluid. On going from low to high altitude, those persons who lost weight and remained well increased their resting ventilation, whereas those who gained weight did not (p = 0.03). This relative hypoventilation in the latter group was confirmed by higher values of Pco2 (heated hand vein blood) and lower values of arterial saturation (ear oximeter) at Pheriche. Vital capacity measured in Kathmandu was correlated with arterial saturation at Pheriche (p = 0.02); persons with low vital capacity were more hypoxemic with more symptoms of AMS. We conclude that relative hypoventilation and weight gain appear early in the development of AMS suggesting links between altitude hypoxia, hyperventilation, hypocapnia, and the body's handling of water.

Acute Disease↗